bdnf - brain derived neurotrophic factor
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Publication
Journal: Genes, brain, and behavior
December/7/2008
Abstract
Brain-derived neurotrophic factor (BDNF) signaling pathways have been shown to be essential for opioid-induced plasticity. We conducted an exploratory study to evaluate BDNF variability in opioid addict responders and nonresponders to methadone maintenance treatment (MMT). We analyzed 21 single nucleotide polymorphisms (SNPs) across the BDNF genomic region. Responders and nonresponders were classified by means of illicit opioid consumption detected in random urinalysis. Patients were assessed by a structured interview (Psychiatric Research Interview for Substance and Mental Disorders (PRISM)-DSM-IV) and personality was evaluated by the Cloninger's Temperament and Character Inventory. No clinical, environmental and treatment characteristics were different between the groups, except for the Cooperativeness dimension (P < 0.001). Haplotype block analysis showed a low-frequency (2.7%) haplotype (13 SNPs) in block 1, which was more frequent in the nonresponder group than in the responder group (4/42 vs. 1/135; P(corrected) = 0.023). Fine mapping in block 1 allows us to identify a haplotype subset formed by only six SNPs (rs7127507, rs1967554, rs11030118, rs988748, rs2030324 and rs11030119) associated with differential response to MMT (global P sim = 0.011). Carriers of the CCGCCG haplotype had an increased risk of poorer response, even after adjusting for Cooperativeness score (OR = 20.25 95% CI 1.46-280.50, P = 0.025). These preliminary results might suggest the involvement of BDNF as a factor to be taken into account in the response to MMT independently of personality traits, environmental cues, methadone dosage and psychiatric comorbidity.
Publication
Journal: Frontiers in behavioral neuroscience
February/19/2019
Abstract
Behavioral or cognitive functions are known to be influenced by thermal stress from the change in ambient temperature (Ta). However, little is known about how increased Ta (i.e., when the weather becomes warm or hot) may affect operant conditioned behavior and the neural substrates involved. The present study thus investigated the effects of high Ta on operant behaviors maintained on a fixed-ratio 1 (FR1) and a differential reinforcement for low-rate responding 10 s (DRL 10-s) schedule of reinforcement. The rats were randomly assigned to three groups receiving acute exposure to Ta of 23°C, 28°C, and 35°C, respectively, for evaluating the effects of high Ta exposure on four behavioral tests. Behavioral responses in an elevated T-maze and locomotor activity were not affected by Ta treatment. Regarding operant tests, while the total responses of FR1 behavior were decreased only under 35°C when compared with the control group of 23°C, those of DRL 10-s behavior were significantly reduced in both groups of 28°C and 35°C. Distinct patterns of inter-response time (IRT) distribution of DRL behavior appeared among the three groups; between-group differences of behavioral changes produced by high Ta exposure were confirmed by quantitative analyses of IRT data. Western blot assays of dopamine (DA) D1 and D2 receptor, DA transporter (DAT) and brain-derived neurotrophic factor (BDNF) were conducted for the sample tissues collected in six brain areas from all the subjects after acute high Ta exposure. Significant Ta-related effects were only revealed in the dorsal hippocampus (dHIP). In which, the DAT levels were increased in a Ta-dependent fashion that was associated with operant behavior changes under high Ta exposure. And, there as an increased level of D1 receptors in the 28°C group. In summary, these data indicate that the performance of operant behavior affected by the present high Ta exposure is task-dependent, and these changes of operant behaviors cannot be attributed to gross motor function or anxiety being affected. The regulation of dHIP DAT may be involved in this operant behavioral change under high Ta exposure.
Publication
Journal: Neuroscience
February/21/2019
Abstract
Brain-derived neurotrophic factor (BDNF) expression and signaling activity in brain are influenced by chronic ethanol and stress. We previously demonstrated reduced Bdnf mRNA levels in the medial prefrontal cortex (mPFC) following chronic ethanol treatment and forced swim stress (FSS) enhanced escalated drinking associated with chronic ethanol exposure. The present study examined the effects of chronic ethanol and FSS exposure, alone and in combination, on Bdnf mRNA expression in different brain regions, including mPFC, central amygdala (CeA), and hippocampus (HPC). Additionally, since microRNA-206 has been shown to negatively regulate BDNF expression, the effects of chronic ethanol and FSS on its expression in the target brain regions were examined. Mice received four weekly cycles of chronic intermittent ethanol (CIE) vapor or air exposure and then starting 72-h later, the mice received either a single or 5 daily 10-min FSS sessions (or left undisturbed). Brain tissue samples were collected 4-h following final FSS testing and Bdnf mRNA and miR-206 levels were determined by qPCR assay. Results indicated dynamic brain regional and time-dependent changes in Bdnf mRNA and miR-206 expression. In general, CIE and FSS exposure reduced Bdnf mRNA expression while miR-206 levels were increased in the mPFC, CeA, and HPC. Further, in many instances, these effects were more robust in mice that experienced both CIE and FSS treatments. These results have important implications for the potential link between BDNF signaling in the brain and ethanol consumption related to stress interactions with chronic ethanol experience.
Publication
Journal: Applied physiology, nutrition, and metabolism = Physiologie appliquee, nutrition et metabolisme
October/30/2019
Abstract
Aerobic exercise may enhance memory in older adults. However, the optimal intensity and underlying mechanism are unclear. This community-based study examined the effect of aerobic exercise intensity on memory and general cognitive abilities. Brain-derived neurotrophic factor (BDNF) was examined as a potential mechanism. Sixty-four sedentary older adults participated in one of three groups: 1) high-intensity interval training (HIIT); 2) moderate continuous training (MCT); or 3) stretching control (CON). Prior to and following the intervention, high-interference memory was assessed using a Mnemonic Similarity task and executive functions were assessed using Go Nogo and Flanker tasks. HIIT led to the greatest memory performance compared to MCT and CON [F(2, 55) = 6.04, p = .004] and greater improvements in memory correlated with greater increases in fitness [rs(46) = .27, p = .03]. Exercise intensity seemed to matter less for executive functioning, as positive trends were observed for both HIIT and MCT. No significant differences in BDNF were found between groups. Overall, these results suggest that aerobic exercise may enhance memory in older adults, with the potential for higher intensity exercise to yield the greatest benefit. While our findings suggest that BDNF does not regulate these adaptations, the mechanisms remain to be determined. Novelty bullets: • High-intensity interval training results in the greatest memory performance in inactive older adults compared to moderate continuous training or stretching • Improvement in fitness correlates with improvement in memory performance.
Publication
Journal: Frontiers in behavioral neuroscience
January/8/2019
Abstract
Background: There is rapidly emerging interest in music interventions in healthcare. Music interventions are widely applicable, inexpensive, without side effects, and easy to use. It is not precisely known how they exert positive effects on health outcomes. Experimental studies in animal models might reveal more about the pathophysiological mechanisms of music interventions. Methods: We performed a systematic review of experimental research in rodents. The electronic databases EMBASE, Medline(ovidSP), Web-Of-Science, PsycINFO, Cinahl, PubMed publisher, Cochrane, and Google scholar were searched for publications between January 1st 1960 and April 22nd 2017. Eligible were English-written, full-text publications on experimental research in rodents comparing music vs. a control situation. Outcomes were categorized in four domains: brain structure and neuro-chemistry; behavior; immunology; and physiology. Additionally, an overview was generated representing the effects of various types of music on outcomes. Bias in studies was assessed with the SYRCLE Risk of Bias tool. A meta-analysis was not feasible due to heterogeneous outcomes and lack of original outcome data. Results: Forty-two studies were included. Music-exposed rodents showed statistically significant increases in neuro-chemistry, such as higher BDNF levels, as well as an enhanced propensity for neurogenesis and neuroplasticity. Furthermore, music exposure was linked with statistically significantly improved spatial and auditory learning, reduced anxiety-related behavior, and increased immune responses. Various statistically significant changes occurred in physiological parameters such as blood pressure and (para)sympathetic nerve activity following music interventions. The majority of studies investigated classical music interventions, but other types of music exerted positive effects on outcomes as well. The SYRCLE risk of bias assessment revealed unclear risk of bias in all studies. Conclusions: Music interventions seem to improve brain structure and neuro-chemistry; behavior; immunology; and physiology in rodents. Further research is necessary to explore and optimize the effect of music interventions, and to evaluate its effects in humans.
Publication
Journal: Brain : a journal of neurology
May/28/2019
Abstract
Dysregulated excitability within the spinal dorsal horn is a critical mediator of chronic pain. In the rodent nerve injury model of neuropathic pain, BDNF-mediated loss of inhibition (disinhibition) gates the potentiation of excitatory GluN2B N-methyl-d-aspartate receptor (NMDAR) responses at lamina I dorsal horn synapses. However, the centrality of this mechanism across pain states and species, as well as the molecular linker involved, remain unknown. Here, we show that KCC2-dependent disinhibition is coupled to increased GluN2B-mediated synaptic NMDAR responses in a rodent model of inflammatory pain, with an associated downregulation of the tyrosine phosphatase STEP61. The decreased activity of STEP61 is both necessary and sufficient to prime subsequent phosphorylation and potentiation of GluN2B NMDAR by BDNF at lamina I synapses. Blocking disinhibition reversed the downregulation of STEP61 as well as inflammation-mediated behavioural hypersensitivity. For the first time, we characterize GluN2B-mediated NMDAR responses at human lamina I synapses and show that a human ex vivo BDNF model of pathological pain processing downregulates KCC2 and STEP61 and upregulates phosphorylated GluN2B at dorsal horn synapses. Our results demonstrate that STEP61 is the molecular brake that is lost following KCC2-dependent disinhibition and that the decrease in STEP61 activity drives the potentiation of excitatory GluN2B NMDAR responses in rodent and human models of pathological pain. The ex vivo human BDNF model may thus form a translational bridge between rodents and humans for identification and validation of novel molecular pain targets.
Publication
Journal: Journal of Taibah University Medical Sciences
November/15/2019
Abstract

Objective
This study aimed to determine the allelic and genotypic association of the Val66Met (rs6265) polymorphism in the BDNF gene with stress levels in preclinical medical students of Universiti Sultan Zainal Abidin (UniSZA), Terengganu, Malaysia.

Methods
In this cross-sectional study, we recruited all 122 preclinical medical students. The validated depression anxiety stress scales-21 (DASS-21) questionnaire was distributed and blood samples were collected from each subject for DNA extraction. Genotyping analysis of the BDNF gene (Val66Met) polymorphism was performed via an optimised polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method.

Results
A total of 105 subjects agreed to participate in this study. Indian students were found to more likely have the Val/Val genotype, whereas Malay students were more likely to have the Met/Met genotype (p = 0.027). Individuals carrying any one of the three BDNF genotypes (Val/Val, Val/Met and Met/Met) differed significantly from each other in terms of their perception of stress (p = 0.010); students carrying the Val/Val genotype (M = 10.6) perceived significantly lower stress than students carrying the Val/Met (M = 14) and Met/Met (M = 15.1) genotypes.

In our study, the Met-allele was associated with higher stress levels. To the best of our knowledge, this is the first study investigating this stress-related gene in medical students. The findings from this study should trigger more investigators to focus on the impact of stress on genetically predisposed medical students.
Publication
Journal: The world journal of biological psychiatry : the official journal of the World Federation of Societies of Biological Psychiatry
November/4/2019
Abstract
Objectives: Synaptic plasticity and brain-derived neurotrophic factor (BDNF) signalling are proposed to play key roles in antidepressant drug action. Ketamine, an N-methyl-D-aspartate receptor antagonist and putative antidepressant, may increase synaptic plasticity in prefrontal cortex through higher expression of BDNF. Furthermore, ketamine was shown to change resting-state functional connectivity (RSFC) of dorsomedial prefrontal cortex (dmPFC).Methods: In a randomised, placebo-controlled study, we investigated acutely (100 min) and at 24 h following subanesthetic ketamine infusion which dmPFC seeded RSFC changes are most strongly associated with plasma BDNF level changes in 53 healthy participants (21 females, age: 24.4 ± 2.9 years) using 7 T-fMRI.Results: We observed higher relative levels of BDNF 2 h and 24 h after ketamine compared to placebo. Whole-brain regression revealed that the change in BDNF after 24 h was associated with RSFC decreases from dmPFC to posterior cingulate cortex and ventromedial PFC at 24 h and exploratively also at the 100 min measurement point. Follow-up analyses revealed that RSFC reductions following ketamine were restricted to subjects showing increased BDNF levels at 24 h.Conclusions: Our findings indicate BDNF level dynamics following ketamine are related to acute and 24 h RSFC changes. Particularly when BDNF increases are observed after ketamine infusion, a disconnection from dmPFC after 24 h is seen and may reflect synaptic plasticity effects.
Publication
Journal: Acta psychiatrica Scandinavica
May/31/2012
Abstract
OBJECTIVE
The aims of this study were to test the individual association of the serotonin transporter gene (SLC6A4), the brain-derived neurotrophic factor gene (BDNF) and the GABA(A) α(6) receptor subunit gene (GABRA6) with anxiety-related traits and to explore putative gene-gene interactions in a Spanish healthy sample.
METHODS
A sample of 937 individuals from the general population completed the Temperament and Character Inventory questionnaire to explore Harm Avoidance (HA) dimension; a subsample of 553 individuals also filled in the Big Five Questionnaire to explore the Neuroticism dimension. The whole sample was genotyped for the 5-HTTLPR polymorphism (SLC6A4 gene), the Val66Met polymorphism (BDNF gene) and the T1521C polymorphism (GABRA6 gene).
RESULTS
Homozygous individuals for the T allele of the T1512C polymorphism presented slightly higher scores for HA than C allele carriers (F = 2.96, P = 0.019). In addition, there was a significant gene-gene interaction on HA between the 5-HTTLPR and Val66Met polymorphisms (F = 3.4, P = 0.009).
CONCLUSIONS
GABRA6 emerges as a candidate gene involved in the variability of HA. The effect of a significant gene-gene interaction between the SLC6A4 and BDNF genes on HA could explain part of the genetic basis underlying anxiety-related traits.
Publication
Journal: Psychiatry research
March/10/2019
Abstract
Brain-derived neurotrophic factor (BDNF) is deemed to be associated with the psychopathology of bipolar I disorder (BD). However, studies focusing on accuracy of BDNF levels to differentiate these patients from healthy controls (HCs) are scarce. Over a discrete twelve-year period, we investigated serum BDNF levels in patients with BD and compared them to age-, sex- and body mass index (BMI)-matched HCs. There were lower serum BDNF levels in 83 samples with BD than in 222 HCs samples (5.7 ± 4.2 ng/ml vs. 12.2 ± 7.5 ng/ml, F = 46.784). Pearson's correlation test showed significant positive correlations between Young Mania Rating Scale scores and the BDNF levels among 61 manic patients (γ = 0.339). The receiver operating characteristic curve analysis showed BDNF levels demonstrated a moderate accuracy of being able to differentiate BD patients from HCs (AUC = 0.801). The most adequate cut-off points of the BDNF level were 6.74 ng/ml (sensitivity = 82.0%, specificity = 63.9%). Our results support that BDNF demonstrated moderate accuracy to distinguish BD patients from HCs. In the future, greater samples would be required to prove these results.
Publication
Journal: Medicine and science in sports and exercise
March/4/2019
Abstract
Aerobic exercise (AEx) exerts antidepressant effects, although the neurobiological mechanisms underlying such effects are not well understood. Reduced brain-derived neurotrophic factor (BDNF) and elevated cortisol have been implicated in the pathophysiology of depression and appear to normalize with antidepressant treatment. Thus, BDNF and cortisol may serve as biological targets for developing AEx as an antidepressant treatment.This study examined the effects of AEx, of different intensities, on serum BDNF and cortisol in individuals with and without depression.Thirteen participants with depression (10 females; age = 27.2 ± 6.9 yr; Montgomery-Äsberg Depression Rating Scale = 21.7 ± 4.7) and 13 control participants (10 females; age 27.2 ± 7.2 yr; Montgomery-Äsberg Depression Rating Scale = 0.5 ± 0.9) participated. Experimental visits consisted of 15 min of low-intensity cycling (LO) at 35% heart rate reserve, high-intensity cycling (HI) at 70% heart rate reserve, or sitting (CON). During each visit, blood samples were obtained at baseline, immediately postexercise (IP), and then every 15 min postexercise for 1 h (15P, 30P, 45P, and 60P). Group, condition, and time differences in BDNF and cortisol were assessed.There were no group differences in cortisol and BDNF. Secondary analysis revealed that BDNF increased in an intensity-dependent nature at IP, and cortisol was significantly elevated at 15P after HI. Changes in BDNF and cortisol showed significant linear relationships with changes in HR.HI AEx can elicit acute, transient increases in BDNF and cortisol in young, healthy, and physically active, nondepressed and mild to moderately depressed individuals. This work suggests that AEx has potential to significantly affect the central nervous system function, and the magnitude of such effect may be directly driven by exercise intensity.
Publication
Journal: International review of neurobiology
October/14/2019
Abstract
Synaptic plasticity is an experience-dependent process that results in long-lasting changes in synaptic communication. This phenomenon stimulates structural, molecular, and genetic changes in the brain and is the leading biological model for learning and memory processes. Synapses are able to show persistent increases in synaptic strength, or long-term potentiation (LTP), as well as persistent decreases in synaptic strength, known as long-term depression (LTD). Understanding the complex interactions that regulate these activity-dependent processes can provide insight for the development of strategies to improve cognitive function. Twenty years ago, we provided the first evidence indicating that aerobic exercise can reliably enhance LTP, and went on to show that it can also regulate some of the mechanisms involved in LTD induction. Since then, several laboratories have confirmed and expanded these findings, helping to identify different molecular mechanisms involved in exercise-mediated changes in synaptic efficacy. This chapter reviews this material and shows how these experimental findings may prove valuable for alleviating the burden of neurodegenerative diseases in an aging population.
Publication
Journal: F1000Research
October/4/2019
Abstract
Complex mechanisms control the signaling of neurotrophins through p75 NTR and Trk receptors, allowing cellular responses that are highly context dependent, particularly in the nervous system and particularly with regard to the neurotrophin brain-derived neurotrophic factor (BDNF). Recent reports describe a variety of sophisticated regulatory mechanisms that contribute to such functional flexibility. Mechanisms described include regulation of trafficking of alternative BDNF transcripts, regulation of post-translational processing and secretion of BDNF, engagement of co-receptors that influence localization and signaling of p75 NTR and Trk receptors, and control of trafficking of receptors in the endocytic pathway and during anterograde and retrograde axonal transport.
Publication
Journal: Behavioral and brain functions : BBF
April/7/2014
Abstract
BACKGROUND
Brain-derived neurotrophic factor (BDNF) has been implicated in the pathogenesis of major depression. Individuals with type 2 diabetes (T2DM) have a high prevalence of major depression and low levels of BDNF. We therefore explored whether the BDNF Val66Met polymorphism is associated with co-morbid depression and whether depression affects the serum levels of BDNF in a Han Chinese subjects with T2DM.
METHODS
A Total of 296 T2DM patients and 70 healthy volunteers (Health control, HC group) were recruited in this study. T2DM patients were divided into two subgroups: depressive diabetes group (DDM group, n = 64) and non-depressive diabetes group (NDDM group, n = 232), according to the presence or the absence of depression assessed by Center for Epidemiologic Studies Depression Scale (CES-D) and Patient Health Questionnaire-9 (PHQ-9). Val66Met polymorphism was detected by polymerase chain reaction-restriction fragment length polymorphism analysis (PCR-RFLP). Serum BDNF levels were measured by ELISA kit.
RESULTS
In this study, 21.6% (64/296) patients with T2DM had depression. The BDNF Val66Met genotype distributions were statistically different among the three groups (χ2 = 7.39, p < 0.05). DDM group carried the highest frequencies of Met allele (53.9%) compared to HC group (39.3%) and NDDM group (38.8%). Subjects with Met/Met had lowest serum BDNF levels (76.59 ± 5.12 pg/ml, F = 7.39, p < 0.05) compared to subjects with Val/Met (79.04 ± 5.19 pg/ml) and Val/Val (83.83 ± 3.97 pg/ml). Within T2DM group, it was also observed that the serum BDNF levels in DDM group were significantly lower than those in NDDM group (76.67 ± 5.35 vs. 79.84 ± 3.97 pg/ml, p < 0.05). In type 2 diabetes subjects, BDNF serum levels were significant correlations with genotypes (r = -0.346, p < 0.01), depression scores (r = -0.486, p < 0.01) and HbA1c (r = -0.168, p < 0.05). After adjustment for gender, HbA1c, BMI and numbers of complications, BDNF Val/Met genotype distributions (OR = 2.105, p < 0.05) and decreased serum BDNF levels (OR = 0.835, p < 0.01) were independently associated with depression in T2DM.
CONCLUSIONS
The BDNF Val66Met polymorphism might be implicated in the pathogenesis of depression in T2DM by decreasing serum BDNF levels in Han Chinese Subjects.
Publication
Journal: Journal of the College of Physicians and Surgeons--Pakistan : JCPSP
March/30/2019
Abstract
To determine the comparative effect of monosialoganglioside versus citicoline on the content changes of serum apoptotic factors (PDCD5, sFas and sFasL), neurological function indices (BDNF, NSE, S100-β and NGF) and oxidative stress indices (SOD, MDA and GSH-PX) in newborns with hypoxic-ischemic encephalopathy (HIE).An experimental study.Emergency Department, Affiliated Children's Hospital of Zhengzhou University, China, from October 2016 to February 2018.A total of 90 newborns with HIE were randomly divided into a treatment group and a control group, with 45 cases in each group. In addition to the conventional treatment, the treatment group was given monosialoganglioside treatment, while the control group was given citicoline treatment. Both groups were treated for 10 days. After treatment, the content differences of serum apoptosis factors (PDCD5, sFas and sFasL), neurological function indices (BDNF, NSE, S100-β and NGF) and oxidative stress indices (SOD, MDA and GSH-PX) were observed in the two groups.After treatment, the levels of serum PDCD5, sFas, sFasL, MDA, NSE and S100-β in the treatment group were lower than those in the control group (all p<0.001). The contents of serum SOD, GSH-PX, BDNF and NGF in the treatment group were higher than those in the control group (all p<0.001).Monosialoganglioside can effectively improve the apoptotic factors, neurological function and oxidative stress indices in newborns and maintain the stability of the internal environment, so it is worthy of promotion and application.
Publication
Journal: The international journal of neuropsychopharmacology
March/26/2019
Abstract
Suicide and major depression are prevalent in individuals reporting early-life adversity. Prefrontal cortex volume is reduced by stress acutely and progressively, and changes in neuron and glia density are reported in depressed suicide decedents. We previously found reduced neurotrophic factor brain-derived neurotrophic factor in suicide decedents and with early-life adversity, and we sought to determine whether cortex thickness or neuron or glia density in the dorsolateral prefrontal and anterior cingulate cortex are associated with early-life adversity or suicide.A total of 52 brains, constituting 13 quadruplets of nonpsychiatric controls and major depressive disorder suicide decedents with and without early-life adversity, were matched for age, sex, race, and postmortem interval. Brains were collected at autopsy and frozen, and dorsolateral prefrontal cortex and anterior cingulate cortex were later dissected, postfixed, and sectioned. Sections were immunostained for neuron-specific nuclear protein (NeuN) to label neurons and counterstained with thionin to stain glial cell nuclei. Cortex thickness, neuron and glial density, and neuron volume were measured by stereology.Cortical thickness was 6% less with early-life adversity in dorsolateral prefrontal cortex and 12% less in anterior cingulate cortex (P < .05), but not in depressed suicide decedents in either region. Neuron density was not different in early-life adversity or with suicide, but glial density was 17% greater with early-life adversity in dorsolateral prefrontal cortex and 15% greater in anterior cingulate cortex, but not in suicides. Neuron volume was not different with early-life adversity or suicide.Reported early-life adversity, but not the stress associated with suicide, is associated with thinner prefrontal cortex and greater glia density in adulthood. Early-life adversity may alter normal neurodevelopment and contribute to suicide risk.
Publication
Journal: Journal of applied oral science : revista FOB
April/10/2019
Abstract
Previous studies suggested that mastication activity can affect learning and memory function. However, most were focused on mastication impaired models by providing long-term soft diet. The effects of chewing food with various hardness, especially during the growth period, remain unknown.To analyze the difference of hippocampus function and morphology, as characterized by pyramidal cell count and BDNF expression in different mastication activities.28-day old, post-weaned, male-Wistar rats were randomly divided into three groups (n=7); the first (K0) was fed a standard diet using pellets as the control, the second (K1) was fed soft food and the third (K2) was fed hard food. After eight weeks, the rats were decapitated, their brains were removed and placed on histological plates made to count the pyramid cells and quantify BDNF expression in the hippocampus. Data collected were compared using one-way ANOVA.Results confirmed the pyramid cell count (K0=169.14±27.25; K1=130.14±29.32; K2=128.14±39.02) and BDNF expression (K0=85.27±19.78; K1=49.57±20.90; K2=36.86±28.97) of the K0 group to be significantly higher than that of K1 and K2 groups (p<0.05); no significant difference in the pyramidal cell count and BNDF expression was found between K1 and K2 groups (p>0.05).A standard diet leads to the optimum effect on hippocampus morphology. Food consistency must be appropriately suited to each development stage, in this case, hippocampus development in post-weaned period.
Publication
Journal: The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry
May/27/2015
Abstract
OBJECTIVE
Brain-derived neurotrophic factor (BDNF) has been considered a risk factor for suicidal behavior in adult populations. BDNF secretion is influenced by epigenetic (DNA promoter methylation) and genetic (val66met polymorphism) profiles. We investigated the independent and interactive effects of BDNF methylation status and val66met polymorphisms on late-life suicidal ideation.
METHODS
In total, 732 Korean community residents aged 65+ years were evaluated; of 639 without suicidal ideation, 579 (90.6%) were followed up 2 years later. The prevalence and incidence of suicidal ideation were ascertained using the Geriatric Mental State Schedule. Sociodemographic and clinical covariates included age, sex, education, depressive symptoms, cognitive function, and disability. The independent effects of BDNF methylation status on the prevalence and incidence of suicidal ideation were investigated using multivariate logistic regression models. The two-way interactions of BDNF methylation status and val66met polymorphism on suicidal ideation were assessed using the same models.
RESULTS
Higher BDNF methylation status was significantly associated with both prevalence and incidence of suicidal ideation, independent of potential covariates. No significant methylation-genotype interaction was found.
CONCLUSIONS
The BDNF hypothesis and the epigenetic origin of the suicidal behavior were supported, even in old age. BDNF promoter methylation status may be useful as a biological marker for suicidality in late life.
Publication
Journal: International journal of environmental research and public health
March/20/2019
Abstract
The purpose of this study was to investigate the effects of regular taekwondo (TKD) training on physical fitness, neurotrophic growth factors, cerebral blood flow (CBF) velocity, and cognitive function in elderly women. Thirty-seven women aged 65 or older were randomly assigned to either TKD (n = 19) or control (n = 18) group. TKD training was performed at 50⁻80% maximum heart rate (HRmax) for 60 min, five times per week for 16 weeks. All participants underwent the following examinations before and after the intervention: Senior Fitness Test; serum levels of neurotrophic growth factors, including brain-derived neurotrophic factor (BDNF), vascular endothelial growth factor (VEGF), and insulin-like growth factor-1 (IGF-1); systolic, diastolic, and mean blood flow velocity and pulsatility index of the middle cerebral artery using Doppler ultrasonography; Mini-Mental State Examination for dementia screening (MMSE-DS); and Stroop Color and Word Test (word, color, and color-word). In the TKD group, lower body strength and flexibility, aerobic endurance levels, BDNF, VEGF, and IGF-1 serum levels as well as the color-word test scores were significantly increased after as compared to before the intervention (p < 0.05). No statistically significant differences were found in cerebral blood flow velocities and the MMSE-DS score (p > 0.05). These findings suggest that regular TKD training may be effective in improving not only fitness but also cognitive function in elderly women. The latter effect may be due to increased neurotrophic growth factor levels.
Publication
Journal: Psychiatry research
April/11/2010
Abstract
We tested for associations between five single nucleotide polymorphisms (SNPs) located in the area containing the Neuregulin 1 gene (NRG1) and three SNPs within the brain-derived neutrophic factor gene (BDNF) in an Italian sample consisting of 171 schizophrenia subjects and 349 controls. No association was found for any of the polymorphisms tested, either in single locus or in haplotype analysis.
Publication
Journal: The Journal of international medical research
February/1/2012
Abstract
Brain-derived neurotrophic factor (BDNF) plays a critical role in many aspects of neuronal biology and hippocampal physiology and pathology, and has been implicated as a potential therapeutic target in temporal lobe epilepsy (TLE). BDNF total mRNA and its six transcripts were compared in the hippocampal tissue of TLE patients with or without hippocampal sclerosis (HS) by real-time fluorescence quantitative polymerase chain reaction. Excitatory actions induced by BDNF on hippocampal cells were investigated by whole-cell patch-clamp recordings. Statistically significant increases in three human BDNF mRNA transcripts were observed in TLE patients with HS compared with those without HS (transcripts 2, 3 and 5 exhibited 2.1-, 2.3- and 4.1-fold increases, respectively); there were no significant increases in other transcripts. BDNF directly induced N-methyl-D-aspartate currents in dentate granule cells of TLE patients with HS. These results demonstrated that BDNF transcripts were selectively upregulated in TLE patients with HS compared with those without HS. Moreover, BDNF induced excitability of dentate granule cells in TLE patients with HS.
Publication
Journal: Journal of psychosomatic research
October/30/2014
Abstract
OBJECTIVE
Coping with cancer is an important determinant of psychological morbidity, quality of life, and treatment adherence in cancer patients. The aim of this study was to elucidate the association between the brain-derived neurotrophic factor (BDNF) Val66Met polymorphism and coping response to stress in patients diagnosed with advanced gastric cancer.
METHODS
Ninety-one subjects (60 males, 31 females) recently diagnosed with advanced gastric cancer were recruited. Coping style and distress level were examined using the Mini-Mental Adjustment to Cancer (Mini-MAC) scale and Hospital Anxiety and Depression Scale, and genotyping was evaluated. To examine the temporal stability of the Mini-MAC scores, a 6-week follow-up evaluation was conducted in 72 patients, after completion of two chemotherapy cycles.
RESULTS
Coping style to cancer significantly differed between the Met carriers of BDNF Val66Met and the Val/Val homozygotes. The Met carriers were significantly more anxious than the Val/Val homozygotes.
CONCLUSIONS
The present findings suggest that the BDNF Val66Met polymorphism may be involved in individual coping responses to cancer. The Met allele of BDNF Val66Met may be predictive of an anxious coping style in patients with advanced cancer.
Publication
Journal: Neurobiology of disease
December/22/2011
Abstract
Mesio-temporal lobe epilepsy (MTLE), the most common drug-resistant epilepsy syndrome, is characterized by the recurrence of spontaneous focal seizures after a latent period that follows, in most patients, an initial insult during early childhood. Many of the mechanisms that have been associated with the pathophysiology of MTLE are known to be regulated by brain-derived neurotrophic factor (BDNF) in the healthy brain and an excess of this neurotrophin could therefore play a critical role in MTLE development. However, such a function remains controversial as other studies revealed that BDNF could, on the contrary, exert protective effects regarding epilepsy development. In the present study, we further addressed the role of increased BDNF/TrkB signaling on the progressive development of hippocampal seizures in the mouse model of MTLE obtained by intrahippocampal injection of kainate. We show that hippocampal seizures progressively developed in the injected hippocampus during the first two weeks following kainate treatment, within the same time-frame as a long-lasting and significant increase of BDNF expression in dentate granule cells. To determine whether such a BDNF increase could influence hippocampal epileptogenesis via its TrkB receptors, we examined the consequences of (i) increased or (ii) decreased TrkB signaling on epileptogenesis, in transgenic mice overexpressing the (i) TrkB full-length or (ii) truncated TrkB-T1 receptors of BDNF. Epileptogenesis was significantly facilitated in mice with increased TrkB signaling but delayed in mutants with reduced TrkB signaling. In contrast, TrkB signaling did not influence granule cell dispersion, an important feature of this mouse model which is also observed in most MTLE patients. These results suggest that an increase in TrkB signaling, mediated by a long-lasting BDNF overexpression in the hippocampus, promotes epileptogenesis in MTLE.
Publication
Journal: The world journal of biological psychiatry : the official journal of the World Federation of Societies of Biological Psychiatry
July/10/2011
Abstract
OBJECTIVE
Val66Met BDNF gene polymorphism is shown to affect the function of mature BDNF and mature BDNF plays an important role in the hippocampal neurogenesis and neuronal survival.
METHODS
A relationship of Val66Met BDNF gene polymorphism and hippocampal volumes in 33 MDD patients and 40 healthy controls is investigated. Region of interest analysis was conducted on the images acquired via MRI.
RESULTS
Depressed patients had smaller left hippocampal volumes compared to healthy controls. The diagnosis of MDD was not significantly related to hippocampal volumes among Met carriers; however, among Val homozygotes depressed patients had significantly smaller left hippocampal volumes compared to controls. Although both right and left hippocampal volumes showed nearly significant correlation with the duration of illness, this correlation reached (negative) significant levels only in the right hippocampal volume of the Val homozygotes.
CONCLUSIONS
Val homozygote genotype may serve as a vulnerability factor in MDD regarding hippocampal volume loss. This finding can be considered as a supportive evidence for the neurotrophic factor hypothesis of depression.
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